ArticlePflugers Archiv : European journal of physiology2008
Functional coupling of Gs and CFTR is independent of their association with lipid rafts in epithelial cells.
Article in Pflugers Archiv : European journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Cross-talk between CFTR and sphingolipids in cystic fibrosis.FEBS open bio · 2023Review
- Lipid-driven CFTR clustering is impaired in cystic fibrosis and restored by corrector drugs.Journal of cell science · 2022Article
- The bidirectional relationship between CFTR and lipids.Communications biology · 2020Review
- Agonists that stimulate secretion promote the recruitment of CFTR into membrane lipid microdomains.The Journal of general physiology · 2019Article
- CFTR gets together.The Journal of general physiology · 2019Article
- Cyclodextrins reduce the ability of Pseudomonas aeruginosa outer-membrane vesicles to reduce CFTR ClAmerican journal of physiology. Lung cellular and molecular physiology · 2019Article
- Phagocytosis depends on TRPV2-mediated calcium influx and requires TRPV2 in lipids rafts: alteration in macrophages from patients with cystic fibrosis.Scientific reports · 2018Article
- Cholesterol modulates CFTR confinement in the plasma membrane of primary epithelial cells.Biophysical journal · 2015Article
- Cholesterol and ion channels.Sub-cellular biochemistry · 2010Review
- Eicosanoid release is increased by membrane destabilization and CFTR inhibition in Calu-3 cells.PloS one · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cystic fibrosis transmembrane conductance regulator (CFTR) has been found to be colocalized with G-protein-coupled receptors (GPCRs) and the downstream signaling molecules; however, the mechanisms of the colocalization remain largely elusive. The present work has investigated the role of lipid rafts in the localized signaling from GPCRs to CFTR. Using commonly used sucrose gradient centrifugation, we found that CFTR along with G(alpha)S was associated with lipid rafts, and the association was disrupted by cholesterol depletion with methyl-beta-cyclodextrin (MCD) treatment in Calu-3 human airway epithelial cells. Using short-circuit current (I (sc)) as a readout of CFTR in Calu-3 cells or T84 human colonic epithelial cells, we showed that MCD, while increasing basal membrane permeability, had no effect on the I (sc) induced by several GPCR agonists. Similar results were also obtained with a cholesterol biosynthesis inhibitor lovastatin and a cholesterol-binding agent filipin in Calu-3 cells. Furthermore, cholesterol depletion did not impair cyclic AMP production elicited by the GPCR agonists in Calu-3 cells. Our data suggest that GPCR-mediated signaling maintain their integrity after lipid raft disruption in Calu-3 and T84 epithelial cells and cast doubts on the role of lipid rafts as signaling platforms in GPCR-mediated signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.